Abstract
Cardiovascular disease is a major cause of morbidity and mortality in patients with hypertension. Epidemiological and clinical studies have shown that damage of large conduit arteries is a major contributory factor [1]. Macrovascular disease develops slowly in hypertensive patients and is responsible for the high incidence of congestive heart failure, left ventricular hypertrophy (LVH), ischemic heart disease, sudden death, cerebrovascular accidents and peripheral artery diseases. Although the most frequent underlying cause of these complications is occlusive lesions due to atheromatous plaques, this aspect represents only one form of the structural response to metabolic and hemodynamic alterations which interfere with the hypertensive process. The spectrum of arterial alterations in hypertension is broader, including large artery hypertrophy associated with hemodynamic burden [2]. The consequences of these alterations may be different from those attributed to the presence of atherosclerotic plaques alone. In this chapter, the basic concepts on changes in arterial structure and function in hypertension are reviewed and their alterations in response to the blockade of the renin-angiotensin system are discussed in experimental and clinical situations.
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Safar, M.E., Boudier, H.A.J.S., Van Bortel, L.M.A.B., London, G.M. (2001). Arterial structure and function and blockade of the renin-angiotensin system in hypertension. In: D’Orléans-Juste, P., Plante, G.E. (eds) ACE Inhibitors. Milestones in Drug Therapy MDT. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-7579-0_8
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